Aktivity of Rhokinase inhibitors, on the oubain induced hipertansive rat vessels

Several studies have shown that chronic administration of ouabain induces hypertension, an effect that seems to be linked to the inhibition of the Na+-K+-ATPase. The smooth muscle contractions by agonists (e.g., 5-HT, phenylephrine) and KCl involve the Ca+2-dependent activation of myosin light chain kinase, and Ca+2 independent rho/rho kinase pathways. Pharmacological manipulation of rho/rho kinase pathway in isolated tissue can be achieved by using fasudil or Y-27632 that inhibits its effector rho-kinase.In this study, our aims are to investigate the role of rho/rho kinase pathways by Y-27632 in ouabain induced hypertension rat thoracic aorta. For these reason we were evaluated firstly, KCl and phenylephrine-induced contractions before and after Y27632 incubations and secondly Y27623 relaxation responses on precontracted arteries with KCl or phenylephrine. Between control and oubain-induced hypertension rat, KCl EC50 value was not change, but Emax value was significantly increased. After Y27623 incubation KCl EC50 value was significantly increase both control and oubain-induced hypertension rat groups. Oubain-induced hypertension rat Emax value was significantly reduced after Y27632 incubation. Phenylephrine contractile response EC50 value was significantly reduced after Y27632 incubation. Also, After Y27632 incubation Emax value of control and oubain-induced hypertension groups was reduced as before Y27632. Y23632 relaxation responses EC50 value was significantly decreased KCl-precontracted arteries as a control group, but significantly increased both EC50 and Emax value in phenylephrine-precontracted arteriesThese results suggest that oubain induced hypertension in aorta, ROCK activation may have a role in this hypertension model.